异种动物血清诱导的大鼠肝纤维化模型及其机制

研究建立免疫性肝纤维化模型，并探讨该模型形成过程中的形态变化特点及模型形成的始动机制。Wistar大鼠腹腔注射猪血清诱导免疫性肝纤维化模型，以光镜和电镜观察肝纤维化不同阶段的形态变化，并计数嗜酸性粒细胞（Eos）和肥大细胞，以免疫荧光法检测肝内IgG和补体C3。结果：①猪血清注射8周后均形成肝纤维化；②肝纤维化形成过程中除肝星状细胞（HSC，原称Ito细胞）增多外，尚发现原始间叶细胞（PMC）增多、活化；③实验早期汇管区及间隔内Eos和肥大细胞增多，IgG和C3阳性，停止注射后逐渐减弱。结论：本模型用于肝纤维化过程的研究较为理想，其发生可能与异种血清引起的Ⅰ型变态反应中迟发相反应有关；除HSC外，原始间叶细胞也是纤维生成细胞的重要来源。

HETEROSERUM-INDUCED RAT LIVER FIBROSIS MODEL AND ITS MECHANISM

PURPOSE To investigate the morphological changes in the process Of heteroserum-induced rat liver fibrosis and the mechanism of fibrogenesis of this model.METHODS A model of heteroserum-induced rat liver fibrosis was established by injected porcine serumintraperitoneally. In addition to the observation of the morphological changes of this model, the infiltration ofeosinophils and mast cells was studied quantitatively and the deposition of IgG and complement C3 was detectedimmunofluorescencely.RESULTS The rat liver fibrosis was induced succeededly at the end of 8 weeks alter injection of heteroserum; besides the increase of hepatic stellated cells during the process of liver fibrosis, proliferation and activation Of primaly mesenchyma cells(PMCs) was also found; in the early stage, infiltration Of eosinophils andmast cells was significantly increased and the despition of IgG and C3 was positive in the portal tracts and sepia,while gradually decreased after stop of injection.CONCLUSIONS This model is more suitable for study liver fibrogenesis, the pathogenesis of this modelmay related with the allergen - induced late phase reaction (LPR) caused by the injection with heteroserum, andthe PMCs as well as hepatic stellated cells are important courses for ECM prepucing cells.